The effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on the incidence and progress of posterior subcapsular opacities (PSO) associated with retinal degeneration are being studied in Royal College of Surgeons (RCS) rats, in which rod photoreceptor outer segment debris accumulates secondary to a phagocytic defect in the retinal pigmented epithelium. Evidence has been obtained that oxidative changes in polyunsaturated fatty acids in the debris lead to water- soluble toxic aldehydes that cen be detected in the vitreous, and are toxic to lens membranes. Several diets prevent the mature cataracts, and dark-rearing prevents the PSO detectable microscopically. Pink-eyed dystrophic rats exposed to constant light of 25 footcandles beginning (1) at 20-23 postnatal days or (2) at birth, had histopathological changes similar to those in some naturally occurring human posterior subcapsular cataracts (PSC), such as in retinitis pigmentosa. Many mature cataracts also occur with cyclic light of low intensity at a time when a large amount of rhodopsin debris is present. In the RCS dystrophic rat, freed retinal may have a prolonged lifetime (owing to slowed conversion of retinal to retinal and to poor regeneration of rhodopsin). Freed retinal may act as a photosensitizer to generate singlet oxygen, highly energetic oxidant for polyunsaturated lipids. Prevention of the cataracts by dark rearing or by feeding a purified diet with lipid-soluble antioxidants (vitamin E, BHT + Beta-carotene) supports the hypothesis of lipoperoxidative damage to the lens. Principles established with this readily manipulated animal model may have significance for slowing or preventing human PSC and mature cataracts.